The initial prognosis was excellent, but within two months the patient had succumbed to her illness. What looked like a simple case of feline herpes virus was actually an insidious presentation of FIP.
It started out like a typical upper respiratory infection: crusty eyes and sneezing in a 10-week-old shelter kitten. She was presenting for her first wellness visit after being adopted two weeks prior. She had already received three FVRCP vaccines through the shelter and tested negative for feline leukemia. At less than three months old, she’d had more veterinary care than most kittens her age. She was showing signs consistent with rhinotrachitis, also known as feline herpes, which is by far the most common cause of upper respiratory infections (URI) in cats and kittens. Rhinotrachitis is the equivalent of the human “cold sore” – appearing during times of stress as nasal congestion and runny eyes – but quickly suppressed by the immune system. It is ubiquitous in kittens from shelter environments. Her veterinarian treated her supportively for this common viral infection of cats with a lysine amino acid supplement and antibiotic eye ointment. She was expected to make a full recovery.
Four weeks later, her symptoms had progressed. Her belly was swollen, her appetite was poor, and she had developed diarrhea. Her symptoms worsened despite antibiotic treatment. Her veterinarian extracted a thick straw-colored fluid from her belly, a grim finding given that abdominal effusion is a tell tale-sign of wet FIP. Given the kitten’s clinical history and the results of tests performed on blood and abdominal fluid – a presumptive diagnosis of FIP was made. At this time, it was unclear if her initial sneezing and crusty eyes were related to her current symptoms. What was heartbreakingly apparent, is that within the span of a few weeks, everything had changed. There would be no recovery. The kitten had days, at most, weeks to live. Treatment included the steroid prednisilone, sub-cutaneous fluids, vitamin B12, feline omega interferon, and the appetite stimulant mirtazapine.
At 17 weeks of age, just over two months after her adoption, the kitten lost her fight against FIP. She was brought to her veterinary clinic exhibiting signs of shock – struggling to breathe with a low body temperature, low heart rate, and pale gums. Given the grave prognosis that accompanies a diagnosis of FIP, the family made the difficult decision to euthanize and spare her further suffering. A necropsy was performed. The findings were surprising and shed light on the origin of her initial upper respiratory infection.
Along with classic signs of wet FIP – abdominal effusion and viral lesions in the classically affected organs – the kitten was found to have a diffuse pyogranulomatous rhinitis. The nasal turbinates – which consist of a spongy maze of bone lined with mucous membranes that warm and humidify air with every breath – had been partially destroyed. Immunohistochemistry identified virus laden macrophages invading the cribeform plate – a porous sieve-like bone that serves as the roof of the nasal cavity. A respiratory PCR performed on pooled postmortem swabs from the conjunctiva, nasal cavity, and oropharynx revealed a low positive for Mycoplasma felis. M. felis is a common respiratory pathogen that can be found in both sick and healthy cats. The panel was negative for all other bacterial pathogens known to cause destruction of the nasal turbinates in cats. No rhinotracheitis virus (feline herpes) was isolated.
Post-mortem testing revealed that FIP had been proliferating in the kitten’s upper respiratory tract. The nasal passages where targeted in what appeared to be the first sign of a lethal systemic infection. Feline coronaviruses are known to cause transient upper respiratory and gastrointestinal symptoms, but this case is unique in that the virus spread extensively throughout the nasal cavity leading to destruction of the delicate nasal turbinates and invasion of the cribeform plate. Despite its presence at this important junction of the blood-brain barrier, the virus was not detected in the kitten’s brain tissue. Sanger sequencing of the important viral S1/S2 activation site revealed a the same mutation associated with FIP was present in all infected tissues.
One of the most important questions to come out of this case study is the role of the upper respiratory tract in the transmission of FIP. The internal mutation theory, which is well accepted in the field, postulates that FIP arises uniquely from mutation of a temperate parent feline enteric coronavirus within EACH infected cat. In an apparent trade off of transmissibility for virulence, FIP loses the ability to infect new hosts through the fecal-oral route. But what happens in cases like that of this kitten, where the upper respiratory tract is infected to the point that the nasal turbinates begin to break down?
- Does a sneeze have the potential to be infectious?
- Does this less common upper respiratory presentation explain outbreak situations that are reported within shelters and catteries?
- Do we need to re-think guidelines for prevention when respiratory signs are involved?
Further study is clearly warranted. This case highlights the potential for upper respiratory signs in FIP and reminds clinicians that rhinitis is a less common and more insidious presentation of this lethal disease.
Curious to read more? This post is a summary of a case study published by Nicole M André, Andrew D Miller, and Gary R Whittaker. Their manuscript, Feline infectious peritonitis virus-associated rhintis in a cat, was first published on June 23, 2020 in the Journal of Feline Medicine and Surgery Open Reports. It is openly available on the publisher’s website – https://journals.sagepub.com/doi/10.1177/2055116920930582